Population movements over space and time played a crucial role in generating the genetic patterns that are observed in the present day. Numerous factors, such as climate changes or cultural innovations, have the potential to induce large-scale movements, such as population expansions (i.e. increases both in density and range) or contractions to refugee areas. It is thus very important to take the spatial dynamic of populations into account when trying to reconstruct their history from genetic data. Computer simulation constitutes a very powerful tool for the study of the combined impacts of biological and demographic factors on the genetic structure of populations. The rapid increase of computer power opens many new possibilities for research in that specific area. A series of recent studies have focused on the consequences of population expansions on their genetic diversity. These studies extensively described one potentially important genetic process which may occur during a range expansion: the “mutation surfing” phenomenon. In this paper, we describe in detail this process and its potential implications for the establishment of the current genetic diversity in Europe. We also discuss the limitations and perspectives of such computer simulation studies in the field, and possible future improvements to them.

[...]

author=Currat.et.al.2012

SE–NW PC1 gradient does not fit a simple expansion from the Near East.

In a subsequent study (Francois et al., 2010), we again simulated a large set of scenarios for the Paleolithic and Neolithic expansions, but this time we generated many virtual genetic samples distributed all over Europe (and not only along a SE–NW transect). Instead of looking at allele frequency clines, we performed principal component analyses in order to check which scenario (combination of parameters) fits the PC1 showing a Southeast–Northwest cline, as described by Menozzi et al. (1978). Our study directly follows the one by Novembre and Stephens (2008), which demonstrated that PC clines similar to those reported by Menozzi et al. (1978) could be recreated by a “null” model of isolation by distance, without any demographic expansion. Our study revealed an unexpected result: in a majority of cases (78%–100%) the PC1 cline is perpendicular to the expansion instead of being parallel to it, at odds with what is commonly thought (Fig. 5). A PC1 parallel to the expansion was almost never obtained. Among the many observations drawn from those simulations, we showed that a single expansion from the Middle East results in PC1 cline oriented from the Iberian Peninsula to Russia, which does not fit at all the SE–NW PC1 cline observed in Europe.

However, this surprising result can be explained by the mutation surfing phenomenon. Indeed, if we look at the frequency pattern in one dimension, along the axis of a population expansion, surfing alleles display an increasing cline of frequency (AFC). But looking at the two dimensions level, different mutations appeared at different places of the wave front, creating sectors along the axis perpendicular to the expansion (Fig. 6). Those sectors correspond to areas where different alleles are fixed or predominant and their presence leads to a very high genetic differentiation along this axis perpendicular to the expansion. In a few words, surfing promotes genetic differentiation along the axis of expansion of a population by increasing the frequency of some alleles, but if the area is broad enough, it also promotes an even larger differentiation pattern that is parallel to the axis of expansion. The formation of such sectors is a phenomenon driven by random fluctuations that originate in a thin band of pioneers at the expanding front and has been confirmed in vitro in bacteria (E. Coli) and yeast populations (Hallatschek et al., 2007).

The consequence of the existence of sectors is that genetic differentiation perpendicular to the axis of an expansion is greater than genetic differentiation along the axis. As the first principal component (PC1) reveals the axis of largest differentiation, in this case the PC1 is a cline perpendicular to the expansion. Using our simulation framework, a SE–NW PC1 gradient was consistently obtained only when an expansion from the Southwest (Iberic peninsula) was simulated at the onset of the last glacial maximum (20,000 years ago), followed by the Neolithic expansion with a very high genetic contribution of local hunter-gatherers (> 80 %). This result deserves more investigation, particularly in conjunction with issues of environmental heterogeneity, but it underlines the need to consider potential retreat to southern refugee areas and postglacial routes in future simulations aiming at reconstructing the evolution of modern humans in Europe.

Very good, JeanL. We know from many years that this is the only truth and it will be demonstrated just after that the powers who are against will be defeated. Test Mangino, and it will be clear where R1b1*/R-M269 was born and expanded.

Very good, JeanL. We know from many years that this is the only truth and it will be demonstrated just after that the powers who are against will be defeated. Test Mangino, and it will be clear where R1b1*/R-M269 was born and expanded.

Sounds like the next edition in the Star Was sequence. Is this the "Return of the Jeddi?"

SE–NW PC1 gradient does not fit a simple expansion from the Near East..... Using our simulation framework, a SE–NW PC1 gradient was consistently obtained only when an expansion from the Southwest (Iberic peninsula) was simulated at the onset of the last glacial maximum (20,000 years ago), followed by the Neolithic expansion with a very high genetic contribution of local hunter-gatherers (> 80 %). This result deserves more investigation, particularly in conjunction with issues of environmental heterogeneity, but it underlines the need to consider potential retreat to southern refugee areas and postglacial routes in future simulations aiming at reconstructing the evolution of modern humans in Europe.

Does this have to do with the R1b Y lineages? What are your key points?

SE–NW PC1 gradient does not fit a simple expansion from the Near East..... Using our simulation framework, a SE–NW PC1 gradient was consistently obtained only when an expansion from the Southwest (Iberic peninsula) was simulated at the onset of the last glacial maximum (20,000 years ago), followed by the Neolithic expansion with a very high genetic contribution of local hunter-gatherers (> 80 %). This result deserves more investigation, particularly in conjunction with issues of environmental heterogeneity, but it underlines the need to consider potential retreat to southern refugee areas and postglacial routes in future simulations aiming at reconstructing the evolution of modern humans in Europe.

Does this have to do with the R1b Y lineages? What are your key points?

First of all, you are quoting that excerpt as if it was written by me, but that is actually part of the study, so I did not write that, just copied and pasted it, so I don’t have any “key points”. As for their simulations, from what I read, they dealt with autosomal dna, and the genetic clines observed in Europe today, and the conclusion was:

Currat.et.al.2012

“Using our simulation framework, a SE–NW PC1 gradient was consistently obtained only when an expansion from the Southwest (Iberic peninsula) was simulated at the onset of the last glacial maximum (20,000 years ago), followed by the Neolithic expansion with a very high genetic contribution of local hunter-gatherers (> 80 %). This result deserves more investigation, particularly in conjunction with issues of environmental heterogeneity, but it underlines the need to consider potential retreat to southern refugee areas and postglacial routes in future simulations aiming at reconstructing the evolution of modern humans in Europe.”

They also took into account the so called mutation surfing phenomenon, and the putative expansion from the near east replacing all Mesolithic lineages, and they concluded that:

Currat.et.al.2012

“ Among the many observations drawn from those simulations, we showed that a single expansion from the Middle East results in PC1 cline oriented from the Iberian Peninsula to Russia, which does not fit at all the SE–NW PC1 cline observed in Europe.

However, this surprising result can be explained by the mutation surfing phenomenon. Indeed, if we look at the frequency pattern in one dimension, along the axis of a population expansion, surfing alleles display an increasing cline of frequency (AFC). But looking at the two dimensions level, different mutations appeared at different places of the wave front, creating sectors along the axis perpendicular to the expansion (Fig. 6). Those sectors correspond to areas where different alleles are fixed or predominant and their presence leads to a very high genetic differentiation along this axis perpendicular to the expansion. In a few words, surfing promotes genetic differentiation along the axis of expansion of a population by increasing the frequency of some alleles, but if the area is broad enough, it also promotes an even larger differentiation pattern that is parallel to the axis of expansion. The formation of such sectors is a phenomenon driven by random fluctuations that originate in a thin band of pioneers at the expanding front and has been confirmed in vitro in bacteria (E. Coli) and yeast populations (Hallatschek et al., 2007).”

SE–NW PC1 gradient does not fit a simple expansion from the Near East..... Using our simulation framework, a SE–NW PC1 gradient was consistently obtained only when an expansion from the Southwest (Iberic peninsula) was simulated at the onset of the last glacial maximum (20,000 years ago), followed by the Neolithic expansion with a very high genetic contribution of local hunter-gatherers (> 80 %). This result deserves more investigation, particularly in conjunction with issues of environmental heterogeneity, but it underlines the need to consider potential retreat to southern refugee areas and postglacial routes in future simulations aiming at reconstructing the evolution of modern humans in Europe.

Does this have to do with the R1b Y lineages? What are your key points?

First of all, you are quoting that excerpt as if it was written by me, but that is actually part of the study, so I did not write that, just copied and pasted it, so I don’t have any “key points”. [...]

SE–NW PC1 gradient does not fit a simple expansion from the Near East.

Yeah, sorry about that! It’s just that when I have to quote long things, I noticed that when I use the [ quote ][ /quote ] feature, the font is far too small, and often times it becomes tedious to read through a long quote with a very small font, so I prefer to not put it in the quote box, and simply just say author=author.et.al.xxxx.

Sounds like the next edition in the Star Wa[r]s sequence. Is this the "Return of the Jeddi?"

1) About the origin of hg. R1b1 and its expansion spoke I and not JeanL, and besides I think that it expanded not from Iberia but from Italy, at least from R-M269 to R-L51. But I have also said that I couldn't exclude that R1b1* was in the Iberian Refugium, given its massive presence in Iberia and in the Isles. The same for R1a-M420, clearly born in Western Europe and not in India (sic!).2) I spoke of "powers" for not saying which they are, in respect to this forum and some friend I have here, but if you know who banned me in the past it won't be difficult to know which they are.

I think that we are back to square one where we started 6 -7 years ago. At that time one of the learned historians on this board was supporting the traditional view of the refugia and the role R1b played in it. David Faux was making similar arguments over other R1b sub-clades. Then came the death knell of the variance model which established a new paradigm, shortened time and capitulation occurred.

Jean L has recently shown that there may be a 3 to 5 factor error in time (shades of Zhivotovsky!) and now shows that the expansion was out of the Iberian refugia (I'll let Machiavelli argue for an Italian refugia).

I have argued, and continue to argue, that variance does not describe the STR mutational process. Rather than deviating from the modal, it appears that the mutations mutate around the modal? The importance of this is that there isn't an increase in variance (significant) with time. When we look at a fast mutator we assume that the one step away is one mutation, the reality is that it possibly 10 to many more mutations. It happened to work for Kerchner and the Ian Cam but thats all, after that you have to emply a new strategy to estimate time and the only one we have left is the set of slow mutators.

I believe we have to reopen the issue of how to estimate TMRCA using Y STR's.

I think that we are back to square one where we started 6 -7 years ago. At that time one of the learned historians on this board was supporting the traditional view of the refugia and the role R1b played in it. David Faux was making similar arguments over other R1b sub-clades. Then came the death knell of the variance model which established a new paradigm, shortened time and capitulation occurred.

Jean L has recently shown that there may be a 3 to 5 factor error in time (shades of Zhivotovsky!) and now shows that the expansion was out of the Iberian refugia (I'll let Machiavelli argue for an Italian refugia).

I have argued, and continue to argue, that variance does not describe the STR mutational process. Rather than deviating from the modal, it appears that the mutations mutate around the modal? The importance of this is that there isn't an increase in variance (significant) with time. When we look at a fast mutator we assume that the one step away is one mutation, the reality is that it possibly 10 to many more mutations. It happened to work for Kerchner and the Ian Cam but thats all, after that you have to emply a new strategy to estimate time and the only one we have left is the set of slow mutators.

I believe we have to reopen the issue of how to estimate TMRCA using Y STR's.

I did not want to intrude in this thread, but JeanL already said this study has to do with autosomal dna, not y-dna. So, we are not "back to square one where we started 6 -7 years ago".

It is not hard to imagine a scenario in which autosomal dna and y-dna have different histories.

Given the apparent confusion, I am thinking of moving this thread to the autosomal subforum.

This is what the authors say about the SE-NW cline in diversity, so it seems they analyzed the PC1 cline of the 38 genetic loci used in Menozzi.et.al.1978 to generate the European clines, if I remember correctly there were up to PC5.

Quote from: Currat.et.al.2012

One genetic pattern commonly observed for Europe is the presence on the continent of clines of allele frequenciesoriented from the southeast to the northwest (SE–NW AFC). Evidence of the presence of such clines was uncovered as early as in 1978 (Menozzi et al.). Those authors created synthetic maps summarizing allelic variation at 38 independent genetic loci, using principal component analyses. Because the first principal component map (PC1) was found to be very similar to the spread of the Neolithic, based on archaeological dates, the authors interpreted those gradients as having been generated by the migration of early farmers from the Near East ~10,000 years ago, and by the subsequent replacement of resident hunter-gatherer populations with little or no interbreeding.

Nonetheless they explored deeply the concept of "surfing mutations" which has been closely linked to R1b in Europe, so all in all it does truly relate to R1b, given that it is amongst one of the allele values which according to many shows a SE-NW diversity distribution.

More from the paper about mutation surfing:

Quote from: Currat.et.al.2012

Population expansion and mutation surfing

[...]

In order to simulate a population expansion, Edmonds et al. (2004) and the authors of subsequent articles (Hallatschek and Nelson, 2008; Klopfstein et al., 2006; Travis et al., 2007) used an original simulation framework (Fig. 2). Briefly, this approach consists of simulating, generation after generation, the evolution of individuals (and their genes) within an array of “demes”, the whole array representing a subdivided population. Each deme represents a population subunit (or subpopulation) that exchanges migrants with its neighbors. The simulation is spatially-explicit in the sense that the array of demes represents a geographic area with known dimensions. At each generation, two steps occur in every deme. First, a demographic regulation step: the local density increases following a logistic equation at a speed dependant on the growth rate (parameter r) until reaching a maximum (parameter K). The carrying capacity K corresponds to the maximum number of individuals that may coexist in one deme given the available resources. Second, a migration step: a proportion of individuals belonging to each deme emigrates to any of the four neighboring demes. This proportion is equal to the migration rate (parameter m). By putting a few individuals in one deme located at one extremity of an empty array and letting the process go on, it is possible to simulate the colonization of a geographic area by a demographically increasing population, and to simulate the genetic diversity of this population throughout the process.

Such frameworks have been used to study the genetic consequences of population range expansions. One important genetic phenomenon resulting from a population expansion is the “mutation surfing” process, which describes a mutation surfing at the wave front of an expanding population. This process has been extensively investigated using computer simulations (Edmonds et al., 2004; Klopfstein et al., 2006) and it describes a mutation (defining a genetic variant or allele) that takes advantage of a population expansion to increase dramatically in frequency, due to the combined effects of genetic drift and demographic growth (Fig. 3). If the allele is neutral (i.e. not the target of natural selection) and if it belongs to the pioneers of a demographic and spatial expansion, it may then surf on this expansion wave. If surfing occurs, the frequency of this mutation drastically increases at the expansion front and, consequently, in the whole population. The final frequency pattern of this neutral allele thus mimics the effect of positive selection. Evaluating the current distribution of a surfing allele may thus lead to the erroneous conclusion that the distribution in question is the result of this allele being the target of positive selection, while it actually results from demographic processes. Klopfstein et al. (2006) demonstrated theoretically that new mutations can reach very high frequencies by surfing, with various final spatial and frequency distributions depending on demographic factors such as population size, growth and migration rates. More importantly, the probability of the survival of a new mutation depends to a large extent on its proximity to the front of the wave. The closer to the front of the expansion wave a mutation is, the higher is the probability that it will surf. This result underlines the very important role played by the pioneers of a population expansion in spreading their genes in the population. When surfing occurs, the centre of the spatial distribution of the mutation is often found far away from its origin, at odds with the common view that the place of origin of an allele is located where its frequency is the highest (Edmonds et al., 2004). It is worth mentioning that surfing is not limited to the mutations that appear during the expansion but affects any standing variants (alleles) carried by the pioneers.

The surfing phenomenon can be explained by three elements associated with the wave front of an expanding population. First, population density at the edge of the expansion is low because the number of individuals colonizing a new area is usually small (Fig. 3A). This promotes genetic drift, i.e. rapid shifts in allele frequency. Second, population density increases after the initial colonization phase, tending to “stabilize” the new allele frequency (Fig. 3B). Third, pioneers in the colonization of the next area are recruited at the wave front and consequently have a higher probability of transmitting their genes farther away (Fig. 3C). The repetition over space and time of these three events can explain why the frequency of some neutral alleles in a population increases during an expansion. Despite the fact that only a small proportion of alleles do actually surf, mutation surfing can have drastic consequences on the evolution of an expanding species (Excoffier and Ray, 2008; Excoffier et al., 2009; Currat and Excoffier, 2004; Currat et al., 2008; Hallatschek et al., 2007). A range expansion can create very complex patterns at neutral loci, mimicking adaptative processes and resembling postglacial segregation of clades from distinct refuge areas. Below, I am going to present the potential implications of mutation surfing with respect to European prehistory.

Sounds like the next edition in the Star Wa[r]s sequence. Is this the "Return of the Jeddi?"

1) About the origin of hg. R1b1 and its expansion spoke I and not JeanL, and besides I think that it expanded not from Iberia but from Italy, at least from R-M269 to R-L51. But I have also said that I couldn't exclude that R1b1* was in the Iberian Refugium, given its massive presence in Iberia and in the Isles. The same for R1a-M420, clearly born in Western Europe and not in India (sic!).2) I spoke of "powers" for not saying which they are, in respect to this forum and some friend I have here, but if you know who banned me in the past it won't be difficult to know which they are.

Follow the alphabet ! M, N, O, P, Q and R, now where in the world can we find M, N, O, P, Q and R ? Of course R is an Asian derived form and R1b1* came from the East to Europe. If you want to find the authentic basal types of R1b1 go to populations like the Bashkirs. You must follow the SNPs' trail just like in any haplogroup, the core is the basal types and the derived types like the Western European types are the peripherical expansion. R1b V88 came from the East to the West just like any other derived type of R1b like M269. Let's face the reality that R1b is just an Eastern Asiatic latecomer in Europe !

Follow the alphabet ! M, N, O, P, Q and R, now where in the world can we find M, N, O, P, Q and R ? Of course R is an Asian derived form and R1b1* came from the East to Europe. If you want to find the authentic basal types of R1b1 go to populations like the Bashkirs. You must follow the SNPs' trail just like in any haplogroup, the core is the basal types and the derived types like the Western European types are the peripherical expansion. R1b V88 came from the East to the West just like any other derived type of R1b like M269. Let's face the reality that R1b is just an Eastern Asiatic latecomer in Europe !

I have already answered your questions many times:1) R-L51+ is Italian (RRocca says between Italy and France: we shall see)2) R-L23 is diffused in Eastern Europe and Middle East, but also in Western Europe, but the subclade L150 (which is also mine) is L150+ in the East but only the Italian Romitti and the British Seymour have the L150-, i.e. the ancestor one. Besides the Eastern L150+ have also other mutations, like L584 etc.3) The ancestor R-M269 is clearly Italian (see the clade with YCAII=17-23 and that with DYS462=12: my cousin Fabrizio Federighi).4) The only intermediate between R1b1 and R-M269 is the Tuscan Mangino (actually Mancini from Monticiano), a R-M269 with the values close to those of R1b1.5) These subclades derive from the Western European R1b1* with YCAII=18-23 and not from the eastern ones with YCAII=23-23 or 21-23. Also R-M335 derives from these Western European R1b1 and not from the Eastern one.6) That the R1b1/V88+ diffused in Africa derives from Middle East and not from Italy (or Spain) by sea is an open question: I am still waiting a paper or a research of Fulvio Cruciani who said to me by a letter (I published on this forum) that the two hypotheses were open also for him.7) The last researches (see Dienekes but also Anatole Klyosov) have many doubts also about the Out of Africa, imagine about your certainties.8) Homo sapiens sapiens entered Europe 45,000 years ago (exactly Italy, if you like), and it isn’t said that many haplogroups thought Eastern ones (like not only R1b (but also R1a) but also G and why not E J etc.) couldn't be the descendants of those men. The aDNA and not your prejudices (like that about G2c I have answered elsewhere) will answer all these questions.

The big game related to the origins of European R1b has already been defined with the cases of R-M343 (R1b* P25 negative) or (R-P25 R1b1* P297 negative and V88 negative). Follow the SNPs. Where are the ancient types of R1b M269 negative in Europe ? If we return to the roots of the R SNP trail we can get the basal types of R* (xR1, xR2) or R1 (xR1a, xR1b) close to the historical sources of the R haplogroup and that's not in Italy, not in the Mediterranean but in the depths of Asia where you came from not long ago ! If you are looking for the origins of the R1b Italian Refugium I would respectfully remember Oscar Wilde: A theologian is like a blind man in a dark room searching for a black cat which isn't there - and finding it!

The big game related to the origins of European R1b has already been defined with the cases of R-M343 (R1b* P25 negative) or (R-P25 R1b1* P297 negative and V88 negative). Follow the SNPs. Where are the ancient types of R1b M269 negative in Europe ? If we return to the roots of the R SNP trail we can get the basal types of R* (xR1, xR2) or R1 (xR1a, xR1b) close to the historical sources of the R haplogroup and that's not in Italy, not in the Mediterranean but in the depths of Asia where you came from not long ago ! If you are looking for the origins of the R1b Italian Refugium I would respectfully remember Oscar Wilde: A theologian is like a blind man in a dark room searching for a black cat which isn't there - and finding it!

We were speaking of R1b1* and subclades and I have a few doubt that the things have gone as I have just said. The issue for your coreligionists was the recent origin of R1b in Europe, not more than 4000 years ago (but we have now an aDNA of almost 5000 years in Europe): first defeat for them.If you speak now of the ancestors I could say:1) R1a-M420 is exclusively European, with at least two clades (the British Pickering and the Italian Celello with some eastern Europeans), and hasn’t been found so far in India or elsewhere in Asia2) R1b, R1, R, or even P etc. could be from Central Asia, but how many years ago? When we go back to the origin of a haplogroup, we see that it is diffused worldwide. We have some R in Africa (see !Kung etc.) like some P in Italy etc. Which is demonstrating this, when the problem was another: the origin of haplogroup R1b1 and R1a in these last thousands of years.3) We had a mongrel here who thought to be an Iranian like your J-M365. Are you yet interested in history?

If you are looking for the origins of the R1b Italian Refugium I would respectfully remember Oscar Wilde: A theologian is like a blind man in a dark room searching for a black cat which isn't there - and finding it!

I completely agree with the great Oscar Wilde, but he was speaking of other. The black cat is “God”, and, as it is known I am completely an atheist, perhaps you should speak to others. And as none is perfect, also Oscar Wilde was searching for something different from me.I am searching not for God, whom I believe invented by man and not the other way around, but for data about which we can do some hypotheses that will be verified or falsified by proofs. I am a scientist and not a theologian.

The issue for your coreligionists was the recent origin of R1b in Europe, not more than 4000 years ago (but we have now an aDNA of almost 5000 years in Europe): first defeat for them.If you speak now of the ancestors I could say:

The issue for your coreligionists was the recent origin of R1b in Europe, not more than 4000 years ago (but we have now an aDNA of almost 5000 years in Europe): first defeat for them.If you speak now of the ancestors I could say:

Which was found in Eastern Germany, not in Italy!

Yes, in the Bell Beaker culture which probably began in Iberia. We will see next where it was born.

Bell Beakers and R1b, that's exactly what everybody has ever expected and presumed. Quite obvious. R1b followed the Atlantic and NW European farming lands with more precipitation and rivers. Go to Western Ireland, the Basque Country and we are going to find the biggest concentrations of R1b in very humid places.What about your Iranian friend, have you seen his M365 SNP in a FTDNA Project ?

For what is worth Mathias Currat is one of the scientists participating in the computational biology simulations of the latest project which is supposed to analyzed a series of archaeological sites dating from 45000 ybp to 4500 ybp in Europe and the Middle East.

PS: It’s a shame that this thread was displaced from the R1b subforum to here simply because it doesn’t deal directly with R1b(yet it deals profoundly with the surfing mutation effect and the diversity gradients of SE-NW, both directly related to R1b), yet threads such as whether the Irish are an admixture or not, or Geoffrey of Monmouth's Historia Regum Britanniae are a good fit for the subforum, while in reality neither one has a direct relationship with R1b, but an indirect one just like this thread. It does say a lot about the objectivity of the subforum.

The "Geoffrey of Monmouth" thread has been moved to General Discussion. The "Irish Admixture" thread, while not having the most accurate title, given its content, has an opening post which makes it clear its creator meant to discuss y haplogroups and especially various clades of R1b.

This topic is NOT directly related to R1b. It deals with European autosomal dna, of which 50% was contributed right off the top by females. Much of the rest of it comes from ancestors who did not belong to y haplogroup R1b. If this thread belongs in the R1b subforum, then certainly duplicates of it belong in every subforum that deals with a y haplogroup found in Europe and in any subforums dealing with mtDNA in Europe.

Better to have this as one single thread in the most fitting subforum for the topic which it treats: autosomal dna.

Please leave moderating and deciding where threads belong to the moderators. Public criticism of those decisions is inappropriate.

This thread is as available for discussion here as it was in the R1b subforum.

It is simply my opinion that this thread has about every right to be in the R1b subforum as any of the Irish autosomal threads, mainly because it deals profoundly with the surfing mutation effect and the diversity gradients of SE-NW, both directly related to R1b. So in a sense, while yes, it is autosomal, the surfing mutation effect is most frequently linked with the frequency pattern observed for R1b in Western Europe, likewise it is often claimed that R1b shows a SE-NW diversity distribution inside of Europe. It doesn't affect me personally if this is included in the R1b subforum or not, after all, I read the article, I gathered what I needed to gather, but the average R1b user is most likely to visit the R1b forum than to visit this subforum, and next time someone brings the surfing mutating argument or the SE-NW diversity patterns, this thread could be useful because they carried simulations assuming different demographic expansions to see how they related to surfing mutations and SE-NW diversity gradients. However, since the thread has been transferred here, it would likely not serve its purpose of educating the public about the surfing mutation effect as tested by computer simulations.